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Physiologic Principles
CVP is the blood pressure within the intrathoracic cranial or caudal
vena cava relative to atmospheric pressure.8 Physiologically, however, ventricular preload is determined by transmural pressure,
which is the difference between intracardiac and extracardiac intrathoracic pressure.10 Therefore, while an increase in intrathoracic
or intrapericardial pressure may cause a decrease in venous return
and subsequently a decrease in preload, it may also lead to an
increase in the CVP. Multiple factors influence transmural pressure, including positive-pressure ventilation, cardiac tamponade,
pleural effusion, and increased intraabdominal pressure.3,10,11
Abstract: Central venous pressure (CVP), an estimate of right atrial pressure, has been used to assess cardiac preload and volume status
in critically ill patients, assist in the diagnosis of right-sided heart failure, and guide fluid resuscitation. It is determined by the interaction
between cardiac function and venous return. CVP measurements are relatively easy to obtain; however, because of the complex
relationship between CVP, cardiac output, and the vascular system, they may be difficult to interpret. This article reviews the physiologic
principles of CVP, indications for its use, technical aspects and pitfalls of CVP measurements, and interpretation of the information obtained.
The use of the cranial versus the caudal abdominal vena cava
for measurement of CVP has been investigated in puppies,12 infants,
and children,13 and studies show that there may be a correlation
between measurements taken from centrally placed catheters in
the cranial intrathoracic and caudal abdominal vena cavae in cats,14
puppies,12 and children.13 However, it has also been demonstrated
that intraabdominal hypertension causes an increase in right atrial
pressure and, therefore, CVP.15 Intraabdominal hypertension
also causes increases in pulmonary artery pressure, systemic vascular
resistance, and pulmonary capillary wedge pressure. These changes,
along with increased CVP, are attributed to catecholamine release
and vascular shifts from the abdominal to the thoracic cavity.15
Common conditions that may lead to abdominal hypertension
include pancreatitis, bile peritonitis, intraabdominal hemorrhage,
large abdominal masses, blunt abdominal trauma, recent abdominal
10
Normal
Depressed
4
-4
12
Figure 2. The relationship between right atrial pressure (or its surrogate, CVP) and
cardiac output (L/min), represented here by the cardiac index (L/min/m2), is not
linear. At low pressures, small increases in CVP may indirectly lead to large
increases in cardiac output via increases in stroke volume. As the curve plateaus,
at high right atrial pressures, even large increases in right atrial pressure (CVP)
have little effect on cardiac output.2
surgery, and fluid resuscitation.16 Despite the correlation demonstrated between measurements taken in the cranial intrathoracic
and caudal intraabdominal vena cavae,12 measurements taken
from the intrathoracic vena cava are preferred. The general recommendation for small animal patients9,17 and human pediatric
patients18 stipulates that the catheter tip lie within the thoracic
cavity when CVP measurements are made.
CVP provides an estimate of right atrial pressure4,8,9,19 and is used
as a surrogate for right ventricular volume at the end of diastole.
Right ventricular end-diastolic volume is proportional to preload,
which is the major determinant of stroke volume at any given
level of contractility.8 Cardiac output is determined by heart rate
and stroke volume, and stroke volume is determined by preload,
afterload, and contractility. The relationship between ventricular
end-diastolic volume and pressure is not linear, but curvilinear
(FIGURE 1 and FIGURE 2). Increasing ventricular end-diastolic volume
(or its surrogate, CVP) by intravenous fluid administration will,
according to the Frank-Starling law, initially lead to increases in
stroke volume and therefore cardiac output. Eventually, however,
further fluid administration leads to increases in end-diastolic
pressure, but no substantial increases in end-diastolic volume or
stroke volume.4,20
CVP is determined by the interaction between cardiac function
and venous return,3 which in turn are influenced by total blood
volume, vascular tone, cardiac output, right ventricular compliance,
and intrathoracic pressure. Right ventricular compliance may
be altered by myocardial and pericardial disorders.8 Ventricular
Principles of Measurement
The animal may be positioned in right lateral, left lateral, or
sternal recumbency; lateral recumbency is preferred. A study by
Oakley and colleagues24 in healthy dogs found no differences in
CVP measurements obtained from animals in left or right lateral
recumbency. For measurement consistency, the patient should
be placed in the same position for each CVP measurement.17
The CVP can be measured using an electronic pressure transducer or a water column manometer. In contrast to electronic
pressure transducers, water manometers may overestimate the
mean CVP by 0.5 to 5 cm H2O.4 These overestimations are partly
due to a meniscus effect of the water column in the manometer
and partly due to observer estimation of a mean CVP value that
naturally fluctuates during inspiration and expiration.25 Over
estimations often vary from patient to patient or from reading to
reading in the same patient even with careful positioning.9 In
critically ill patients, continuous evaluation of CVP using an
electronic pressure transducer connected to the central venous
catheter by a short stiff tube may be more accurate in assessing
rapidly changing trends and responses to fluid boluses.9,25
ECG
P
a
CVP
Systole
c
x
Diastole
Figure 5. Supplies needed for water manometer (Medex manometer set, Smiths
Medical, London). Not shown: central venous catheter, 20-gauge needle, and
string or tape measure.
Three-way stopcock
6- to 20-mL syringe filled with saline
String or tape measure
in series with the central venous catheter and the syringe or fluid
bag. With the stopcock turned off to the manometer, prime the
fluid line and the extension set with fluid to remove any air bubbles.
In order to make the measurement more reproducible, the stopcock should rest on the floor or the bottom of the cage (FIGURE 6).
Assess the patency of the catheter by allowing fluid from the syringe
or saline bag to flow freely into the catheter. If a multilumen central
catheter is used, infusions of fluids through other lumens should be
discontinued before obtaining a CVP reading, as they may artificially increase the measurement.30
Before CVP can be measured with a water manometer, identify
the zero point on the manometer that corresponds to the patients
right atrium. This measurement will need to be subtracted from the
reading to obtain the correct CVP. When the patient is in lateral
recumbency, the sternum serves as a reference point for the right
atrium. For a patient in sternal recumbency, the scapulohumeral
joint or the point of the shoulder is a good reference point. To find
the zero point on the manometer, draw a perpendicular line from
the reference point on the patient to the manometer using the
string or tape measure (FIGURE 6). For a small dog, the zero point
is usually 2 to 3 cm H2O. Therefore, if the column of water in the
manometer equilibrates at 10 cm H2O and the zero point is 2 cm
H2O, the actual CVP would be 8 cm H2O.
To obtain a measurement, fill the manometer with saline
significantly above the expected patient CVP. Turn the three-way
stopcock so that the column of saline in the manometer is continuous with the central catheter and the stopcock is off to the
saline bag or syringe. The saline in the manometer will decrease
until the hydrostatic pressure in the column equilibrates with the
hydrostatic pressure of the blood at the tip of the central catheter.
Once the saline in the manometer stops falling, it has reached the
Figure 6. (A) Measurement of CVP using water manometer. (B) Perpendicular line from the patient to the manometer denoting zero point.
set
Pressure bag
Bag of saline
Examination gloves
Drape
Interpretation
CVP has been used to assess cardiac preload and volume status,3,26
to optimize right ventricular preload,2 and to monitor fluid therapy
in an attempt to minimize the risk of volume overload in patients
with oliguric renal failure or heart failure.9 In addition, CVP has
been advocated as a means to monitor fluid resuscitation in patients
with noncardiogenic shock1,4 and to assess patients for recurrent
pericardial effusion and right-sided heart failure.4,19 A survey of
human criticalists showed that many relied on cardiac filling pressures such as CVP and pulmonary artery occlusion pressure to
help guide fluid therapy.32
Accurate assessment of preload and volume status is vital to the
appropriate management of critically ill patients.9 Unfortunately,
direct measurement of right and left ventricular end-diastolic
pressures requires the use of invasive techniques such as placement
Volume unresponsive
Volume responsive
Pra
Figure 8. Fluid responsiveness demonstrating Starlings law. In the volume-responsive portion of the curve, a change in CVP will produce a measurable change in
cardiac output. Once the plateau phase is reached, additional fluids will no longer
increase cardiac output.1 Pra = right atrial pressure, Q = cardiac output.
Figure 9. Interaction of the return function and cardiac function curves for the
determination of right atrial pressure (Pra) or its surrogate, CVP, and cardiac
output (Q).3 The graphs in the lower left corner show low CVP with high cardiac
function and normal blood volume and return function or with normal cardiac
function but decreased volume. The graphs in the lower right corner show that a
high CVP may be associated with normal return function but decreased cardiac
function or normal cardiac function with high return function because of excess
volume. This explains why a single CVP value alone may not explain cardiac
function or volume status.3 Reproduced with permission from Magder S. How to
use central venous pressure measurements. Curr Opin Crit Care 2005;11:264-270.
Figure 10. (A) A normal CVP tracing. (B) A CVP tracing showing a cannon a wave
(asterisk), which is produced when atrial contraction occurs against a closed
tricuspid valve. Reproduced with permission from Barbeito A, Mark JB. Arterial
and central venous pressure monitoring. Anesthesiol Clin 2006;(24)717-735.
while CVP can be and has been used to assess preload and volume
responsiveness, it may not always be reliable. Clinicians must
recognize situations and factors that may cause CVP to fall short
of its intended use.
CVP has been used in resuscitative efforts in patients with
septic shock and as an indicator of preload in patients with hypovolemia.1,4 It is used as an end point of resuscitation for humans
in septic shock, as illustrated in the landmark study done by Rivers
et al.1 However, CVP may not be an accurate indicator of acute
blood loss. In humans, acute hypovolemia due to blood loss may lead
to a decrease in ventricular compliance and an increase in CVP,
making CVP measurements less reliable during trauma resuscitation.41 Although CVP generally decreases when blood volume
is reduced, as illustrated in a study by Haskins et al,42 an animal
with life-threatening hypovolemia may have a normal CVP.9,41
CVP and other invasive cardiac measurements, such as pulmonary capillary wedge pressure, have been used to aid in the
assessment of patients with heart disease.43 A markedly increased
CVP in a person with acute congestive heart failure confirms
myocardial failure. However, the CVP measurement is rarely
useful to guide fluid therapy or treatment in these patients.44 In dogs,
congestive heart failure is more commonly caused by valvular
disease.45 Regardless of the underlying etiology, the effect of fluid
administration on patients in congestive heart failure remains a
concern. Invasive monitoring, including pulmonary capillary
wedge pressure (PCWP) and CVP, has been used to try to tailor
this therapy. A PCWP represents the pressure in the pulmonary
venous circulation, and readings over 18 mm Hg have been shown
to be consistent with pulmonary edema formation.44 PCWP represents filling pressures affecting the left side of the heart, whereas
the CVP represents the right-sided filling pressures. While there
may be a close relationship between CVP and PCWP in healthy
individuals,21,44 CVP measurements may not represent pulmonary
venous pressure in patients with left-sided congestive heart failure.22
This is because the ability of the right and left ventricles to receive
and pump blood is different in congestive heart failure.22 The filling
pressure of the right ventricle (CVP) may not accurately reflect the
effects of volume infusion on the left ventricle and the pulmonary
circulation.18 Also, the effects of therapy must also be considered.
For example, it is not uncommon for human patients in heart failure
receiving diuretic therapy to have a low CVP and high PCWP.18
Conclusion
The relationship between right atrial pressure, CVP, right ventricular
pressure, right ventricular end-diastolic volume, stroke volume,
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3 CE Credits
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